Advancements in the Study of Biologic Agents in Comorbidities of Psoriasis: A Literature Review

Abstract

This literature review systematically searched relevant literature from the past 10 years using various medical databases, including PubMed, Medline, Cochrane, China National Knowledge Infrastructure (CNKI), Wanfang, and Weipu. As a chronic inflammatory disease, psoriasis is associated with various cells and cytokines of the body's immune system, making them more susceptible to various systemic comorbidities than the general population. At a time when conventional regimens are ineffective and there is a lack of personalized treatment options for such comorbidities, the development of biologics has revolutionized the treatment of psoriasis comorbidities, and a number of biologic combination therapies have been incorporated into first-line treatments in many countries. The focus of this review was to investigate the relationship between psoriasis and comorbidities, such as metabolic syndrome, psoriatic arthritis, cardiovascular diseases, mental disorders, infectious diseases, digestive system diseases, and renal diseases. Furthermore, the study explored the significance of biologic therapies in the management of these comorbidities. Also this paper suggests current conditions and precautions for the use of biologic therapies to minimize the occurrence of adverse effects. This review was performed to provide guidance for clinical drug selection in patients with psoriasis and comorbidities, as well as serve as a reference for the development and application of biologic therapies.

Advances in biologic therapy for the treatment of moderate to severe psoriasis: a systematic review

“…Biologic therapies for moderate to severe psoriasis have seen significant advancements, particularly with the introduction of TNF-α inhibitors, IL-12 and IL-23 inhibitors, and IL-17 and IL-23 pathway inhibitors (Wang et al, 2023). Firstgeneration biologics such as etanercept, infliximab, and adalimumab have transformed psoriasis management by neutralizing TNF-α, a crucial cytokine in the inflammatory cascade.…”